Effect of a staphylococcin on Neisseria gonorrhoeae.
Phage group 2 staphylococcal strain UT0002 contains a large 56S virulence plasmid with genes that code for both exfoliative toxin and a specific staphylococcin termed Bac R(1). Four penicillinase-producing strains and three penicillin-susceptible strains of Neisseria gonorrhoeae were killed by Bac R(1). After 30 min of growth of the penicillin-resistant TR1 strain in 62.5 arbitrary units of Bac R(1) per ml, loss of viability was approximately 90%, and, after 5 h, an approximately 99.99% loss of viability was observed. Lysis did not accompany cell death, and 84% of the Bac R(1) added to the growth medium was adsorbed to the gonococcal cells. The extracellular supernatant fluid from a substrain of staphylococcal strain UT0002 cured of the plasmid for Bac R(1) production had no lethal effect on the gonococcal strains. Bac R(1) was also shown to have bactericidal activity against an L-form of N. meningitidis, indicating that the outer envelope of a neisserial cell is not needed for bacteriocin activity. Ten different normal human sera were unable to neutralize Bac R(1) activity. The bacteriocin lacks adsorption specificity. It binds to but does not kill Escherichia coli cells, indicating that the cell envelope of gram-negative organisms can provide protection against the staphylococcin. (+info)
UK-18892, a new aminoglycoside: an in vitro study.
UK-18892 is a new aminoglycoside antibiotic, a derivative of kanamycin A structurally related to amikacin. It was found to be active against a wide range of pathogenic bacteria, including many gentamicin-resistant strains. The spectrum and degree of activity of UK-18892 were similar to those of amikacin, and differences were relatively minor. UK-18892 was about twice as active as amikacin against gentamicin-susceptible strains of Pseudomonas aeruginosa. Both amikacin and UK-18892 were equally active against gentamicin-resistant strains of P. aeruginosa. There were no appreciable differences in the activity of UK-18892 and amikacin against Enterobacteriaceae and Staphylococcus aureus. Cross-resistance between these two antimicrobials was also apparent. (+info)
Emergence of vancomycin resistance in Staphylococcus aureus. Glycopeptide-Intermediate Staphylococcus aureus Working Group.
BACKGROUND: Since the emergence of methicillin-resistant Staphylococcus aureus, the glycopeptide vancomycin has been the only uniformly effective treatment for staphylococcal infections. In 1997, two infections due to S. aureus with reduced susceptibility to vancomycin were identified in the United States. METHODS: We investigated the two patients with infections due to S. aureus with intermediate resistance to glycopeptides, as defined by a minimal inhibitory concentration of vancomycin of 8 to 16 microg per milliliter. To assess the carriage and transmission of these strains of S. aureus, we cultured samples from the patients and their contacts and evaluated the isolates. RESULTS: The first patient was a 59-year-old man in Michigan with diabetes mellitus and chronic renal failure. Peritonitis due to S. aureus with intermediate resistance to glycopeptides developed after 18 weeks of vancomycin treatment for recurrent methicillin-resistant S. aureus peritonitis associated with dialysis. The removal of the peritoneal catheter plus treatment with rifampin and trimethoprim-sulfamethoxazole eradicated the infection. The second patient was a 66-year-old man with diabetes in New Jersey. A bloodstream infection due to S. aureus with intermediate resistance to glycopeptides developed after 18 weeks of vancomycin treatment for recurrent methicillin-resistant S. aureus bacteremia. This infection was eradicated with vancomycin, gentamicin, and rifampin. Both patients died. The glycopeptide-intermediate S. aureus isolates differed by two bands on pulsed-field gel electrophoresis. On electron microscopy, the isolates from the infected patients had thicker extracellular matrixes than control methicillin-resistant S. aureus isolates. No carriage was documented among 177 contacts of the two patients. CONCLUSIONS: The emergence of S. aureus with intermediate resistance to glycopeptides emphasizes the importance of the prudent use of antibiotics, the laboratory capacity to identify resistant strains, and the use of infection-control precautions to prevent transmission. (+info)
Acinetobacter bacteremia in Hong Kong: prospective study and review.
The epidemiological characteristics of 18 patients with acinetobacter bacteremia were analyzed. Patients (mean age, 55.5 years) developed bacteremia after an average of 14.1 days of hospitalization. Fifteen of 16 patients survived bacteremia caused by Acinetobacter baumannii. Cultures of blood from the remaining two patients yielded Acinetobacter lwoffii. Most patients (78%) resided in the general ward, while four patients (22%) were under intensive care. Genotyping by arbitrarily primed polymerase chain reaction analysis and the temporal sequence of isolation were more useful than phenotyping by antimicrobial susceptibility in the determination of the source of bacteremia, and the intravascular catheter was the leading infection source (39% of cases). The possibility of an association of glucose with the pathogenesis of acinetobacter infection was raised. (+info)
A new rapidly growing mycobacterial species, Mycobacterium murale sp. nov., isolated from the indoor walls of a children's day care centre.
Scotochromogenic mycobacterial isolates from water-damaged parts of indoor building materials of a children's day care centre represented a phenetically and genetically distinct group of strains. A 16S rDNA dendrogram (1243 bp) showed that the closest species to the new strain MA112/96T was Mycobacterium abscessus. Phylogenetic and phenetic analyses (100 characteristics) grouped the new isolates with M. abscessus, Mycobacterium vaccae, Mycobacterium aurum and Mycobacterium austroafricanum. Ribotyping with Pvull restriction distinguished the 5 isolates from the other 12 most closely related species by the major bands at 6.5-7 kb and 13-15 kb. The cell morphology of the new isolates was typical of mycobacteria, electron microscopy revealed a triple-layered cell wall with an irregular electron-dense outer layer. They grew at 10-37 degrees C, with no growth at 45 degrees C in 5 d. The gene encoding the secreted 32 kDa protein, specific to mycobacteria, was detected by PCR. The main whole-cell fatty acids were characterized by high tuberculostearic acid 10Me-C18:0 (17% at 28 degrees C), which increased with increasing growth temperature (22% at 37 degrees C). The other main fatty acids were C18:1 cis9 and C16:0 (21-20% each), followed by, C17:1 cis9 (14%), C16:1 cis10 (8%) and also a high amount of C20 alcohol (9%). alpha-Mycolic acids, keto-mycolates and wax esters were present (C60-C90), MK-9(H2) (90%) and MK-8(H2) were the main menaquinones. The cellular phospholipids were phosphatidylethanolamine, phosphatidylinositol, phosphatidyl inositolmannosides and diphosphatidylglycerol. Polyamine content was low. G+C content was 72.9 mol%. The new isolates are proposed as a new species, Mycobacterium murale sp. nov. The type strain is MA112/96T (= DSM 44340T). (+info)
Emergence of multidrug-resistant Salmonella enterica serotype Typhimurium phage-type DT104 among salmonellae causing enteritis in Israel.
The relative frequency of salmonella strains isolated from hospitalized and non-hospitalized patients in Southern Israel changed during the period, 1994-6. Salmonella enterica serotype Typhimurium definitive phage-type 104 (DT104) appeared in Israel in 1994 and became the most prevalent strain in 1996. An outbreak of enteritis due to Salmonella enterica serotype Agona occurred in Israel, in October 1994 and lasted for 4 months. The relative frequency of Salmonella enterica serotype Enteritidis remained almost constant during these years, with seasonal fluctuations only. The importance of the increase in the prevalence of Typhimurium DT104 has been the epidemic spread of a multiresistant strain of R-type ACT (A, ampicillin; C, chloramphenicol; T, tetracycline) belonging to this phage-type. Since 1995 the frequency of Typhimurium DT104 isolates that possess, in addition to the above R-type, a chromosomally encoded resistance to the quinolone drug, nalidixic acid, increased tenfold. In 1996, 27% of the Typhimurium DT104 isolates were of R-type ACTN. S. Enteritidis exhibited over 95% susceptibility to at least eight of the most commonly used antibiotic drugs, and none of the isolates was resistant to quinolone or fluoroquinoline. (+info)
Apicularens A and B, new cytostatic macrolides from Chondromyces species (myxobacteria): production, physico-chemical and biological properties.
A novel macrolide, apicularen A, was produced by several species of the genus Chondromyces. Initially it was discovered by bioassay-guided RP-HPLC-fractionation of culture extracts of Chondromyces robustus, strain Cm a13. Apicularen A showed no antimicrobial activity, but was highly cytotoxic for cultivated human and animal cells, with IC50 values ranging between 0.1 and 3 ng/ml. A cometabolite of apicularen A, the N-acetylglucosamine glycoside apicularen B, was distinctly less cytotoxic with IC50 values between 0.2 and 1.2 microg/ml, and showed weak activity against a few Gram-positive bacteria. Apicularen A is chemically closely related to the salicylihalamides A and B from the marine sponge Haliclona sp. (+info)
BE-31405, a new antifungal antibiotic produced by Penicillium minioluteum. I. Description of producing organism, fermentation, isolation, physico-chemical and biological properties.
A new antifungal antibiotic, BE-31405, was isolated from the culture broth of a fungal strain, Penicillium minioluteum F31405. BE-31405 was isolated by adsorption on high porous polymer resin (Diaion HP-20), followed by solvent extraction, precipitation and crystallization. BE-31405 showed potent growth inhibitory activity against pathogenic fungal strains such as Candida albicans, Candida glabrata and Cryptococcus neoformans, but did not show cytotoxic activity against mammalian cells such as P388 mouse leukemia. The mechanism studies indicated that BE-31405 inhibited the protein synthesis of C. albicans but not of mammalian cells. (+info)